scholarly journals Pure Motor Stroke Secondary to Cerebral Infarction of Recurrent Artery of Heubner after Mild Head Trauma: A Case Report

2016 ◽  
Vol 4 (1) ◽  
pp. 139-141
Author(s):  
Ali Yilmaz ◽  
Zahir Kizilay ◽  
Ayca Ozkul ◽  
Bayram Çirak
Keyword(s):  
Ischemic Stroke ◽  
Head Trauma ◽  
Distal Part ◽  
Brain Mri ◽  
Artery Occlusion ◽  
Acute Ischemia ◽  
Post Traumatic ◽  
The Brain ◽  
Perforating Arteries ◽  
Pure Motor

BACKGROUND: The recurrent Heubner's artery is the distal part of the medial striate artery. Occlusion of the recurrent artery of Heubner, classically contralateral hemiparesis with fasciobrachiocrural predominance, is attributed to the occlusion of the recurrent artery of Heubner and is widely known as a stroke syndrome in adults. However, isolated occlusion of the deep perforating arteries following mild head trauma also occurs extremely rarely in childhood.CASE REPORT: Here we report the case of an 11-year-old boy with pure motor stroke. The brain MRI showed an acute ischemia in the recurrent artery of Heubner supply area following mild head trauma. His fasciobrachial hemiparesis and dysarthria were thought to be secondary to the stretching of deep perforating arteries leading to occlusion of the recurrent artery of Heubner.CONCLUSION: Post-traumatic pure motor ischemic stroke can be secondary to stretching of the deep perforating arteries especially in childhood.

scholarly journals Three-dimensional cultured mesenchymal stem cells enhance repair of ischemic stroke through inhibition of microglia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yuejiao Li ◽  
Yankai Dong ◽  
Ye Ran ◽  
Yanan Zhang ◽  
Boyao Wu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Ischemic Stroke ◽  
Proinflammatory Cytokines ◽  
Infarct Volume ◽  
Brain Lesion ◽  
Three Dimensional ◽  
Artery Occlusion ◽  
Rna Seq ◽  
The Brain

Abstract Background We show previously that three-dimensional (3D) spheroid cultured mesenchymal stem cells (MSCs) exhibit reduced cell size thus devoid of lung entrapment following intravenous (IV) infusion. In this study, we determined the therapeutic effect of 3D-cultured MSCs on ischemic stroke and investigated the mechanisms involved. Methods Rats underwent middle cerebral artery occlusion (MCAO) and reperfusion. 1 × 106 of 3D- or 2D-cultured MSCs, which were pre-labeled with GFP, were injected through the tail vain three and seven days after MCAO. Two days after infusion, MSC engraftment into the ischemic brain tissues was assessed by histological analysis for GFP-expressing cells, and infarct volume was determined by MRI. Microglia in the lesion were sorted and subjected to gene expressional analysis by RNA-seq. Results We found that infusion of 3D-cultured MSCs significantly reduced the infarct volume of the brain with increased engraftment of the cells into the ischemic tissue, compared to 2D-cultured MSCs. Accordingly, in the brain lesion of 3D MSC-treated animals, there were significantly reduced numbers of amoeboid microglia and decreased levels of proinflammatory cytokines, indicating attenuated activation of the microglia. RNA-seq of microglia derived from the lesions suggested that 3D-cultured MSCs decreased the response of microglia to the ischemic insult. Interestingly, we observed a decreased expression of mincle, a damage-associated molecular patterns (DAMPs) receptor, which induces the production of proinflammatory cytokines, suggestive of a potential mechanism in 3D MSC-mediated enhanced repair to ischemic stroke. Conclusions Our data indicate that 3D-cultured MSCs exhibit enhanced repair to ischemic stroke, probably through a suppression to ischemia-induced microglial activation.

Abstract 166: Endothelial Overexpression of LOX-1 Increases Stroke Size in vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Alexander Akhmedov ◽  
Remo D Spescha ◽  
Francesco Paneni ◽  
Giovani G Camici ◽  
Thomas F Luescher
Keyword(s):  
Endothelial Cells ◽  
Ischemic Stroke ◽  
Endothelial Dysfunction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Oxidized Ldl ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
The Brain

Background— Stroke is one of the most common causes of death and long term disability worldwide primarily affecting the elderly population. Lectin-like oxidized LDL receptor 1 (LOX-1) is the receptor for oxidized LDL identified in endothelial cells. Binding of OxLDL to LOX-1 induces several cellular events in endothelial cells, such as activation of transcription factor NF-kB, upregulation of MCP-1, and reduction in intracellular NO. Accumulating evidence suggests that LOX-1 is involved in endothelial dysfunction, inflammation, atherogenesis, myocardial infarction, and intimal thickening after balloon catheter injury. Interestingly, a recent study demonstrated that acetylsalicylic acid (aspirin), which could prevent ischemic stroke, inhibited Ox-LDL-mediated LOX-1 expression in human coronary endothelial cells. The expression of LOX-1 was increased at a transient ischemic core site in the rat middle cerebral artery occlusion model. These data suggest that LOX-1 expression induces atherosclerosis in the brain and is the precipitating cause of ischemic stroke. Therefore, the goal of the present study was to investigate the role of endothelial LOX-1 in stroke using experimental mouse model. Methods and Results— 12-week-old male LOX-1TG generated recently in our group and wild-type (WT) mice were applied for a transient middle cerebral artery occlusion (MCAO) model to induce ischemia/reperfusion (I/R) brain injury. LOX-1TG mice developed 24h post-MCAO significantly larger infarcts in the brain compared to WT (81.51±8.84 vs. 46.41±10.13, n=7, p < 0.05) as assessed morphologically using Triphenyltetrazolium chloride (TTC) staining. Moreover, LOX-1TG showed higher neurological deficit in RotaRod (35.57±8.92 vs. 66.14±10.63, n=7, p < 0.05) and Bederson tests (2.22±0.14 vs. 1.25±0.30, n=9-12, p < 0.05) - two experimental physiological tests for neurological function. Conclusions— Thus, our data suggest that LOX-1 plays a critical role in the ischemic stroke when expressed at unphysiological levels. Such LOX-1 -associated phenotype could be due to the endothelial dysfunction. Therefore, LOX-1 may represent novel therapeutic targets for preventing ischemic stroke.

Head Injuries: A New Treatment for the Post-Concussive Syndrome

1947 ◽  
Vol 93 (391) ◽  
pp. 303-317 ◽  
Author(s):  
Helen S. E. Murray ◽  
H. Halstead
Keyword(s):  
Head Trauma ◽  
Head Injuries ◽  
Personality Change ◽  
The Past ◽  
Traumatic Neurosis ◽  
Symptom Complex ◽  
Post Traumatic ◽  
New Treatment ◽  
Persistent Disability ◽  
The Brain

Gunshot and shrapnel wounds of the head during the war have produced various disabilities not commonly seen in the injuries of peace-time.The symptom complex which usually appears subsequent to head trauma has become very familiar during the past few years. The resemblance from case to case of certain sequelae to head injuries has been grouped together in syndromes, variously labelled post-concussive syndrome, post-traumatic personality change, post-traumatic neurosis and post-contusional state, all indicating an oft-recurring persistent disability following concussion of the brain.

scholarly journals P2Y6 receptor inhibition aggravates ischemic brain injury by reducing microglial phagocytosis

2019 ◽  
Author(s):  
Ruoxue Wen ◽  
Hui Shen ◽  
Shuxian Huang ◽  
Liping Wang ◽  
Zongwei Li ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Myosin Light Chain ◽  
Artery Occlusion ◽  
Walking Test ◽  
Microglial Phagocytosis ◽  
Tnf Α ◽  
Severity Scores ◽  
P2y6 Receptor ◽  
Cerebral Artery Occlusion ◽  
The Brain

Abstract Background Clearance of damaged cells is beneficial for the functional recovery after brain injury. Phagocytosis of tissue and cell debris is an important function of microglia during the development and pathological diseases. However, which specific phagocytic receptor mediates microglial phagocytosis after ischemic stroke is obscure. Methods ICR mice (n=59) underwent 90 minutes transient middle cerebral artery occlusion. P2Y6R, Iba1, GFAP and Tuj-1 double immunostainings were performed to determine P2Y6 receptor location. MRS2578 was injected into mice to inhibit P2Y6 receptor activity. Iba1 and TUNEL staining were performed to examine microglia phagocytosis. Modified neurological severity scores and Grid walking test were used to evaluate the neurological function after ischemic stoke. The expression of IL-1 α, IL-1 β, IL-6, IL-10, TNF-α, TGF-β and MPO was used to examine the inflammation response in the brain. Results The expression of P2Y6 receptor in microglia increased within three days after transient middle cerebral artery occlusion. Inhibition of microglial phagocytosis by the selective inhibitor MRS2578 enlarged the brain atrophy and edema volume after ischemic stroke, subsequently aggravated neurological function using modified neurological severity scores and Grid walking test. MRS2578 treatment had no effect on the expression of IL-1α, IL-1β, IL-6, IL-10, TNF-α, TGF-β and MPO after ischemic stroke, which suggested that it had no effect on the inflammation in the brain. Finally, we found that the expression of myosin light chain kinase decreased after microglial phagocytosis inhibition in ischemic mice, which suggested that myosin light chain kinase was involved in P2Y6 receptor mediated phagocytosis. Conclusion Our results indicated that the P2Y6 receptor mediated microglial phagocytosis played an important role during the acute stage of ischemic stroke, which was a potential target for ischemic stroke treatment.

scholarly journals Image-based stroke rat brain atrophy volume and infarct volume computation

2020 ◽  
Vol 76 (12) ◽  
pp. 10090-10121
Author(s):  
Yung-Kuan Chan ◽  
Chun-Fu Hong ◽  
Meng-Hsiun Tsai ◽  
Ya-Lan Chang ◽  
Ping-Hsuan Sun
Keyword(s):  
Ischemic Stroke ◽  
Rat Brain ◽  
Brain Slice ◽  
Infarct Volume ◽  
Brain Slices ◽  
Artery Occlusion ◽  
Tetrazolium Chloride ◽  
Rat Brain Slice ◽  
Cerebral Artery Occlusion ◽  
The Brain

Abstract Stroke is one of the leading causes of death as well as results in a massive economic burden for society. Stroke is a cerebrovascular disease mainly divided into two types: ischemic stroke and hemorrhagic stroke, which, respectively, refer to the partial blockage and bleeding inside brain blood vessels. Both stroke types lead to nutrient and oxygen deprivation in the brain, which ultimately cause brain damage or death. This study focuses on ischemic stroke in rats with middle cerebral artery occlusion (MCAO) as experimental subjects, and the volumes of infarct and atrophy are calculated based on the brain slice images of rat brains stained with 2,3,5-triphenyl tetrazolium chloride. In this study, a stroke rat brain infarct and atrophy volumes computation system (SRBIAVC system) is developed to segment the infarcts and atrophies from the rat brain slice images. Based on the segmentation results, the infarct and atrophy volumes of a rat brain can be computed. In this study, 168 images of brain slices cut from 28 rat brains with MCAO are used as the test samples. The experimental results show that the segmentation results obtained by the SRBIAVC system are close to those obtained by experts.

Abstract 3048: Real-World Clinical Use of CT Perfusion for Diagnosis and Prediction of Lesion Growth in Acute Ischemic Stroke

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Branko N Huisa ◽  
William P Neil ◽  
Nhu T Bruce ◽  
Marcel Maya ◽  
Benedict Pereira ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Real World ◽  
Cerebral Blood Volume ◽  
Ct Perfusion ◽  
Medical Center ◽  
Brain Mri ◽  
Academic Medical Center ◽  
Acute Ischemia ◽  
Perfusion Maps

Background: Diffusion-weighted imaging (DWI) detects acute ischemia with a high sensitivity. In research centers, qualitative CT perfusion (CTP) mapping correlates well with DWI and may accurately differentiate the infarct core from ischemic penumbra. The value of the CTP in real-world clinical practice, however, has not been fully established. We investigated the yield of CTP - derived cerebral blood volume (CBV) and mean transient time (MTT) for the detection of cerebral ischemia in a sample of acute ischemic stroke (AIS) patients. Methods: In a large metropolitan academic medical center that is a certified Primary Stroke Center (PSC) we retrospectively studied 162 patients who presented between January 2008 and July 2010 with symptoms suggestive of AIS. All patients had an initial Code Brain protocol including non-contrast head CT, CTP, and CTA. As clinically indicated, some patients underwent follow up brain MRI within 48 hours. Acute perfusion maps were derived in real time by a trained operator. From the obtained images CBV, MTT and DWI lesion volumes were manually traced using planimetry (ImageJ v1.42) by two stroke neurologists blinded to clinical information. Volumes were calculated using the Cavaleri theorem. Sensitivity, specificity and statistical analysis were calculated using Graph Pad 5.0. Results: Of 162 patients with acute stroke-like symptoms, 73 had DWI lesions. The sensitivity and specificity to detect abnormal DWI signals were 23% and 100%, for CBV; and 43.8% and 98.9% for MTT. For DWI lesions ≥5ml the yield was 59.3% for CVB and 77.8% for MTT. For lesions ≥10ml the yield was 68.4% for CBV and 89.5% for MTT. In patients with NIHSS ≥5, CBV predicted abnormal DWI in 22.6% and MTT in 35.5%. In patients with NIHSS ≥10, CBV and MTT, both had a yield of 50.0%. A CBV - MTT mismatch of >25% predicted MRI lesion extension in 81.25% of the cases. There were small but significant correlations for DWI versus CBV lesion volumes ( r 2 0.32, P= 0.0001), and for DWI versus MTT lesion volumes ( r 2 0.29, P <0.0001). Correlation between DWI and perfusion maps for MCA territory infarcts were CBV ( r 2 0.3, P <0.0001) and MTT ( r 2 0.45, P <0.0001). Conclusions: In real-world deployment during a Code Brain protocol in a busy PSC, acute imaging with CTP did not predict DWI lesions on brain MRI with sufficient accuracy. In patients with large lesions the predictive value was better.

scholarly journals The KCa3.1 Blocker TRAM-34 Reduces Infarction and Neurological Deficit in a Rat Model of Ischemia/Reperfusion Stroke

2011 ◽  
Vol 31 (12) ◽  
pp. 2363-2374 ◽  
Author(s):  
Yi-Je Chen ◽  
Girija Raman ◽  
Silke Bodendiek ◽  
Martha E O'Donnell ◽  
Heike Wulff
Keyword(s):  
Ischemic Stroke ◽  
Rat Model ◽  
Neurological Deficit ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Beneficial Effects ◽  
Inflammatory Damage ◽  
Male Wistar Rats ◽  
Cerebral Artery Occlusion ◽  
The Brain

Microglia and brain infiltrating macrophages significantly contribute to the secondary inflammatory damage in the wake of ischemic stroke. Here, we investigated whether inhibition of KCa3.1 (IKCa1/KCNN4), a calcium-activated K+ channel that is involved in microglia and macrophage activation and expression of which increases on microglia in the infarcted area, has beneficial effects in a rat model of ischemic stroke. Using an HPLC/MS assay, we first confirmed that our small molecule KCa3.1 blocker TRAM-34 effectively penetrates into the brain and achieves micromolar plasma and brain concentrations after intraperitoneal injection. Then, we subjected male Wistar rats to 90 minutes of middle cerebral artery occlusion (MCAO) and administered either vehicle or TRAM-34 (10 or 40 mg/kg intraperitoneally twice daily) for 7 days starting 12 hours after reperfusion. Both compound doses reduced infarct area by ∼50% as determined by hematoxylin & eosin staining on day 7 and the higher dose also significantly improved neurological deficit. We further observed a significant reduction in ED1+-activated microglia and TUNEL-positive neurons as well as increases in NeuN+ neurons in the infarcted hemisphere. Our findings suggest that KCa3.1 blockade constitutes an attractive approach for the treatment of ischemic stroke because it is still effective when initiated 12 hours after the insult.

A Comparative Study of Brain Perfusion Single-Photon Emission Computed Tomography and Magnetic Resonance Imaging in Patients with Post-traumatic Anosmia

2009 ◽  
Vol 23 (4) ◽  
pp. 409-412 ◽  
Author(s):  
Saeid Atighechi ◽  
Hadi Salari ◽  
Mohammad Hossein Baradarantar ◽  
Rozita Jafari ◽  
Ghasem Karimi ◽  
...  
Keyword(s):  
Single Photon ◽  
Brain Mri ◽  
Photon Emission ◽  
Brain Perfusion ◽  
Emission Computed Tomography ◽  
Control Groups ◽  
Post Traumatic ◽  
Single Photon Emission Computed ◽  
The Brain ◽  
Photon Emission Computed Tomography

Background Loss of smell is a problem that can occur in up to 30% of patients with head trauma. The olfactory function investigation methods so far in use have mostly relied on subjective responses given by patients. Recently, some studies have used magnetic resonance imaging (MRI) and single-photon emission computed tomography (SPECT) to evaluate patients with post-traumatic anosmia. The present study seeks to detect post-traumatic anosmia and the areas in the brain that are related to olfactory impairment by using SPECT and MRI as imaging techniques. Methods The study was conducted on 21 patients suffering from head injury and consequently anosmia as defined by an olfactory identification test. Two control groups (traumatic normosmic and nontraumatic healthy individuals) were selected. Brain MRI, qualitative and semiquantitative SPECT with 99mtc-ethyl-cysteinate-dimer were taken from all the patients. Then the brain SPECT and MRI were compared with each other. Results Semi-quantitative assessment of the brain perfusion SPECT revealed frontal, left parietal, and left temporal hypoperfusion as compared with the two control groups. Eighty-five percent of the anosmic patients had abnormal brain MRI. Regarding the MRI, the main abnormality proved to be in the anterior inferior region of the frontal lobes and olfactory bulbs. Conclusions The findings of this study suggest that damage to the frontal lobes and olfactory bulbs as shown in the brain MRI and hypoperfusion in the frontal, left parietal, and left temporal lobes in the semiquantitative SPECT corresponds to post-traumatic anosmia. Further neurophysiological and imaging studies are definitely needed to set the idea completely.

Abstract TP42: Risk of Acute Ischemic Stroke in Monocular Vision Loss of Vascular Etiology

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jason Zhang ◽  
Lucy Y Zhang ◽  
Jared Matthews ◽  
Danielle Rudich ◽  
David Greer ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Vision Loss ◽  
Brain Mri ◽  
Central Retinal Artery Occlusion ◽  
Brain Magnetic Resonance Imaging ◽  
Retinal Artery Occlusion ◽  
Artery Occlusion ◽  
Monocular Vision ◽  
Neurologic Deficits ◽  
Retinal Artery

Purpose: To evaluate the risk of concurrent acute cortical ischemic stroke in the setting of monocular vision loss of vascular etiology. Design: Retrospective and prospective, cross-sectional study. Subjects: Patients age 18 or older diagnosed with monocular vision loss of suspected or confirmed vascular etiology who had no other neurologic deficits and who received brain magnetic resonance imaging (MRI) within 7 days of onset of visual symptoms. Methods: Medical record review was performed from 2013-2016 at Yale-New Haven Hospital. Subjects were included if vision loss was unilateral, permanent or transient, and thought to be due to a vascular etiology such as central retinal artery occlusion (CRAO) or branch retinal artery occlusion (BRAO). Any subjects with neurologic deficits other than vision loss were excluded. Other exclusion criteria were positive visual phenomena, non-vascular intraocular pathology, and intracranial pathology other than ischemic stroke. Institutional Review Board/Ethics Committee approval was obtained. Main Outcome Measures: Presence or absence of acute cortical stroke on diffusion weighted imaging (DWI) sequence on brain MRI. Results: A total of 641 records were reviewed, with 293 subjects found to have monocular vision loss. After excluding subjects with focal neurologic deficits, there were 41 subjects who met inclusion criteria and received a brain MRI. 8 of the 41 subjects (19.5%) were found to have brain MRI positive for acute cortical strokes. The proportion of lesion positive MRI was 1/23 (4.3%) in transient monocular vision loss subjects, 4/12 (33.3%) in patients with CRAO, and 2/5 (40%) in BRAO. Conclusions: Patients with transient or permanent monocular vision loss of vascular etiology such as CRAO or BRAO may have up to 19.5% risk of concurrent cortical ischemic stroke, even when there are no other neurologic deficits. This highlights the importance of urgent stroke evaluation in this patient population.

Abstract WP322: Do Mural Cells Differentiate Into Microglia-Like Cells After Ischemic Stroke?

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yao Yao ◽  
Abhijit Nirwane
Keyword(s):  
Ischemic Stroke ◽  
Substantial Reduction ◽  
Transgenic Animals ◽  
Artery Occlusion ◽  
Lineage Tracing ◽  
Future Research ◽  
Mural Cells ◽  
Reporter Mice ◽  
Cerebral Artery Occlusion ◽  
The Brain

Introduction: Controversial results exist on whether mural cells can differentiate into microglia-like cells after ischemic stroke. This discrepancy can be due to different experimental methods (immunostaining versus lineage tracing) and/or distinct transgenic animals (RGS5 GFP versus Tbx18-CreERT mice). Methods: To determinate whether mural cells are able to differentiate into microglia-like cells after ischemic stroke, we permanently labeled mural cells with tdTomato by crossing PDGFRβ-Cre and PDGFRβ-CreERT with Ai14 reporter mice. The resulting Ai14:PDGFRβ-Cre + and Ai14:PDGFRβ-CreERT + mice were subjected to 45 minutes of middle cerebral artery occlusion (MCAO) followed by reperfusion. At various time points after injury, the proliferation, apoptosis, and differentiation of PDGFRβ + cells were examined. Results: In both Ai14:PDGFRβ-Cre + and Ai14:PDGFRβ-CreERT + mice, we observed a substantial reduction of PDGFRβ + cells at day 2 after ischemic stroke and a subsequent repopulation (mainly due to proliferation) of PDGFRβ + cells at day 7 after ischemic stroke. We also showed that PDGFRβ + cells changed their morphology and differentiated into microglia-like cells at day 7 after injury, suggesting that PDGFRβ + cells can indeed differentiate into microglia-like cells after ischemic stroke. In addition, we noted that PDGFRβ also labeled Col1α1 + fibroblasts in the brain. Interestingly, high numbers of PDGFRβ + Col1α1 + cells were found in both Ai14:PDGFRβ-Cre + and Ai14:PDGFRβ-CreERT + mice at day 7 after ischemic injury. Conclusions: These results suggest that PDGFRβ is not an ideal marker for mural cells in pathological conditions that involve fibroblast activation. It remains unclear whether mural cells or fibroblasts differentiate into microglia-like cells after ischemic stroke. Future research should focus on answering this important question.

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